Michael Radetsky1. 1. From the Department of Pediatrics, University of New Mexico School of Medicine, Presbyterian Medical Center, Albuquerque, New Mexico.
Abstract
BACKGROUND: Fulminant bacterial meningitis is a rare host reaction to infection characterized by sudden onset, rapid deterioration, abrupt cerebral edema and refractory intracranial hypertension associated with an extremely high mortality rate. METHODS: A search of all relevant medical literature since 1900 was conducted to clarify the nature of this entity and its medical management. RESULTS: Fulminant meningitis occurs in a small percentage of all cases of bacterial meningitis, at all ages and with all infecting organisms. The mortality rate exceeds 50%. Descriptions of fulminant bacterial meningitis are found in medical literature from the preantibiotic era. Its incidence and clinical character have not changed since the introduction of antibiotics and advanced intensive care medicine. The explosive cerebral edema cannot be predicted, and the underlying molecular pathophysiology remains poorly understood. Vigorous neuroresuscitation and the use of adjunctive techniques to control the cerebral edema have not been shown to modify the extreme intracranial hypertension and risk of herniation. CONCLUSION: Fulminant bacterial meningitis is an example of an aberrant host response to infection that challenges available medical intervention.
BACKGROUND: Fulminant bacterial meningitis is a rare host reaction to infection characterized by sudden onset, rapid deterioration, abrupt cerebral edema and refractory intracranial hypertension associated with an extremely high mortality rate. METHODS: A search of all relevant medical literature since 1900 was conducted to clarify the nature of this entity and its medical management. RESULTS:Fulminant meningitis occurs in a small percentage of all cases of bacterial meningitis, at all ages and with all infecting organisms. The mortality rate exceeds 50%. Descriptions of fulminant bacterial meningitis are found in medical literature from the preantibiotic era. Its incidence and clinical character have not changed since the introduction of antibiotics and advanced intensive care medicine. The explosive cerebral edema cannot be predicted, and the underlying molecular pathophysiology remains poorly understood. Vigorous neuroresuscitation and the use of adjunctive techniques to control the cerebral edema have not been shown to modify the extreme intracranial hypertension and risk of herniation. CONCLUSION: Fulminant bacterial meningitis is an example of an aberrant host response to infection that challenges available medical intervention.